3. HYPERTHERMIA
HEAT RELATED ILLNESSES
â¸Broad range of ĂŚtiology and manifestations
â¸Primary disorder due to failure of thermal homeostasis
â¸But hyperthermia may be a secondary disorder
â¸Major causes of hyperthermia are:
â¸Exercise-associated collapse (EAC)
â¸Heatstroke
â¸Drug related heat illness
4. HYPERTHERMIA
PATHOPHYSIOLOGY OF
HYPERTHERMIA
â¸Core body temperature >41.5°C
â¸Progressive denaturing of vital cellular proteins
â¸Failure of vital energy-producing processes
â¸Loss of cellular membrane function
â¸Organ dysfunction:
â¸rhabdomyolysis, APO, DIC, cardiovascular dysfunction,
electrolyte disturbance, renal failure, liver failure, permanent
neurological damage.
5. HYPERTHERMIA
EXERCISE-ASSOCIATED COLLAPSE
â¸Most common heat-related illness at sporting events
â¸Manifests at end of a race
â¸Muscle pump enhanced venous return ceases and cardiac
output drops.
â¸Leads to collapse, often with brief LOC
â¸Due primarily to failure of prompt baroreceptor responses
and not haemodynamically significant dehydration (rare).
6. HYPERTHERMIA
HEATSTROKE
â¸Hallmark is failure of the hypothalamic thermostat
â¸Leading to hyperthermia and organ dysfunction
â¸Exertional heatstroke due to exercise in a thermally
stressful environment
â¸Classic heatstroke occurs in patients with impaired
thermostatic regulation
8. HYPERTHERMIA
SEROTONIN SYNDROME
â¸Serotonin toxicity: the effects are a consequence of a relative excess of central nervous system serotonin.
â¸Dose related, selective serotonin re-uptake inhibitors (SSRIs), lithium, pethidine, monoamine oxidase
inhibitors (MAOIs) and amphetamines.
â¸Clinical diagnosis characterised by CNS, autonomic & motor dysfunction
â¸Develops after a latent period, usually of a few hours, but may be several days
â¸Most patients are only mildly affected and may escape clinical detection.
â¸Severe cases with hyperthermia with muscular rigidity with complications of rhabdomyolysis, DIC, and
renal failure.
â¸Most cases resolve within 24â48hr once the precipitant is withdrawn.
â¸Even in severe cases, the underlying biochemical abnormality rapidly improves, usually with the institution of
muscular paralysis.
â¸Mortality & morbidity is due to the complications of the syndrome
9. HYPERTHERMIA
NEUROLEPTIC MALIGNANT SYNDROME
â¸Neuroleptic malignant syndrome: dopamine depletion or dopamine receptor blockade is
responsible
â¸Rare idiosyncratic reaction to neuroleptic agents with an incidence of between 0.02%
and 3.0% Manifests in patients who recently started or increased neuroleptic treatment
â¸Associated with almost all antipsychotics (both first and second generation)
â¸Reported in patients in whom a dopaminergic agent has been rapidly withdrawn (e.g. in
Parkinsonism).
â¸Latent period of onset of several hours to days.
â¸Four classic signs: fever, rigidity, altered mental state and autonomic instability.
â¸Only the more severe cases develop hyperthermia and its complications.
10. HYPERTHERMIA
MALIGNANT HYPERTHERMIA
â¸Due to exposure to volatile anaesthetic agents or suxamethonium
â¸Malignant hyperthermia is a genetically inherited disorder in
which triggering agents cause a release of sarcoplasmic Ca2+
stores.
â¸Elevated levels of myoplasmic Ca2+
stimulates many
intercellular processes, including glycolysis, muscle contraction
and an uncoupling of oxidative phosphorylation. Leading to
hyperthermia that is purely peripheral in origin.
11. HYPERTHERMIA
RISK FACTORS FOR
HEATSTROKE
⸠Behavioural
⸠Army Recruits
⸠Athletes
⸠Exertion
⸠Inappropriate exposure to high heat
&/or humidity
⸠Babies left in cars
⸠Manual workers
⸠Pilgrims
16. HYPERTHERMIA
PREVENTION OF HEATSTROKE
â¸Education of at risk groups
â¸Exertional heatstoke is most often in short, high intensity
exercise where marked dehydration is unlikely.
â¸Dehydration is not as important as previously thought
â¸Exercise in high heat and humidity environments should be
limited.
17. HYPERTHERMIA
CLINICAL FEATURES OF EXERCISE-
ASSOCIATED COLLAPSE (EAC)
â¸Nausea, vomiting, malaise, dizziness
â¸History of collapse
â¸Tachycardia (likely) and orthostatic hypotension
â¸Core temperature <40°C
â¸Neurological function rapidly returns to normal
18. HYPERTHERMIA
CLINICAL FEATURES OF HEAT STROKE
â¸Neurological dysfunction
â¸Loss of consciousness is a constant feature
â¸Core temperature >41.5°C
â¸Hot dry skin
â¸Profuse sweating is a more common feature than previously
believed
â¸Other features include, tachycardia, hyperventilation, seizures,
vomiting and hypotension
20. HYPERTHERMIA
TREATMENT FOR EXERCISE-
ASSOCIATED COLLAPSE (EAC)
â¸Rapidly responds to supine posture (lying down), rest, and
oral fluids
â¸IV rehydration rarely required
â¸May worsen hyponatraemia due to fluid overload
â¸It increases ADH levels
21. HYPERTHERMIA
TREATMENT FOR HEATSTROKE
â¸Medical emergency!!! Early recognition and early treatment
decrease morbidity and mortality.
â¸Need aggressive cooling of 0.1°C/min
â¸Remove clothing, fine mist spray, ice packs neck, axilla & groin
â¸Iced water immersion, ice slush, cool water immersion, iced
peritoneal lavage and drugs (paralysis with ventilatory support)
â¸IV fluids should be used judiciously
â¸Monitor UEC & clotting closely
22. HYPERTHERMIA
TREATMENT FOR DRUG RELATED
HYPERTHERMIA
â¸Serotonin syndrome
â¸Cool them +/- paralysis
â¸Chlorpromazine (12.5â50 mg IM/IV)
â¸Cyproheptadine (4â8 mg orally 8-hourly).
â¸NMS
â¸Bromocriptine 2.5â10 mg tds. (May reduce the duration)
â¸Malignant hyperthermia
â¸Dantrolene 15-30mg/kg IV
â¸Cease precipitating agent
â¸Full support
23. HYPERTHERMIA
PROGNOSIS
â¸Maximum core temperature and duration of temperature
elevation are predictors of outcome.
â¸Prolonged coma and oliguric renal failure are poor prognostic
signs.
â¸Mortality is still about 10%, but survivors will not suffer long-
term sequelae.
â¸Heat stroke should be referred to ICU
â¸EAC should recover in SSU of ED or onsite
25. HYPOTHERMIA
DEFINITION
â¸Hypothermia: Core temperature < 35°C
â¸Mild (32â35°C)
â¸Thermogenesis is still possible
â¸Moderate (29â32°C)
â¸Progressive failure of thermogenesis
â¸Severe (<29°C)
â¸Poikilothermic and increasing risk of malignant cardia
arrhythmias
26. HYPOTHERMIA
ĂTIOLOGY
â¸Elderly are at greater risk of hypothermia because of reduced metabolic heat
production and impaired responses to a cold environment.
â¸Alcohol is a common ĂŚtiological factor and acts via:
â¸Cutaneous vasodilatation
â¸Altered behavioural responses
â¸Impaired shivering
â¸Hypothalamic dysfunction.
â¸Hypothermia in the ED setting is often associated with underlying infection
27. HYPOTHERMIA
ĂTIOLOGY: âIN ANY SEASON OR
SETTINGâ
â¸Environmental
â¸Cold, wet, windy ambient conditions
â¸Cold water immersion
â¸Exhaustion
â¸Trauma
â¸Multitrauma (entrapment, resuscitation, head injury)
â¸Minor trauma and immobility (e.g. #NOF, #NOH)
â¸Major burns
â¸Drugs
â¸Ethanol
â¸Sedatives (e.g. benzodiazepines) in overdose
â¸Phenothiazines (impaired shivering)
â¸Neurological
â¸CVA
â¸Paraplegia
â¸Parkinsonâs disease
â¸Endocrine
â¸Hypoglycaemia
â¸Hypothyroidism
â¸Hypoadrenalism
â¸Systemic illness
â¸Sepsis
â¸Malnutrition
33. HYPOTHERMIA
CARDIAC RHYTHM IN HYPOTHERMIA
â¸Shivering artefact on ECG
â¸In severe hypothermia typically
this is slow atrial fibrillation
â¸Extra positive deflection in the
QRS (the J or Osborn wave)
in leads II, V3âV6 with
worsening hypothermia.
â¸With handling or may
spontaneously degenerate into
VF or asystole
36. HYPOTHERMIA
MANAGEMENT - FLUIDS
â¸Preferential substrate to generate heat by shivering is muscle
glycogen
â¸Oral glucose may be appropriate in mild hypothermia
â¸In severe hypothermia, gastric stasis and ileus are common
â¸Glucose IV: 5% dextrose IVI 200 ml/hr
â¸Gentle warm IV fluid resuscitation due to relative dehydration as
vascular beds dilate with rewarming
â¸Severe hypotension at 37°C is a normal physiological state at 27°C.
37. HYPOTHERMIA
MANAGEMENT - INTERVENTIONS
â¸Intubation where needed allows protection of the airway and an avenue of rewarming via the
ventilator
â¸AF - should correct with warming alone
â¸no need for chemical correction
â¸Pulse VT/VF; manage along conventional pathways
â¸If DC shocks do not work; repeat every 1°C warmer
â¸Mg2+ may be the anti arrhythmic of choice
â¸Pacing
â¸Transcutaneous pacing may be indicated in a bradycardic patient whose blood pressure is too
low to allow arteriovenous rewarming
â¸Due to cardiac irritability, transvenous pacing is contraindicated in hypothermia
38. HYPOTHERMIA
MANAGEMENT - DRUGS
â¸Pharmacokinetics/Pharmacodynamics change with temperature.
ie insulin is inactive <30°C, thus hyperglycaemia is common in
hypothermia
â¸Drug metabolism of drugs is decreased and protein binding may
be increased in hypothermia.1
â¸With rewarming drugs may become bioavailable at toxic levels.
â¸It may be prudent not to give vasoactive drugs to a patient with
core temperature less than 30C
39. HYPOTHERMIA
MANAGEMENT - WARMING
â¸Stop them becoming cold/colder
â¸Remove wet clothing
â¸Avoid drafts, and multiple
exposures of the patient once
warming has begun
â¸Endogenous rewarming
â¸Warm, dry, wind-free environment
â¸Warmed intravenous fluids (to
prevent cooling)
â¸External exogenous rewarming
â¸Hot bath immersion
â¸Forced-air blankets
â¸Heat packs
â¸Body-to-body contact
â¸Core exogenous rewarming
â¸Warmed, humidified inhalation
â¸Left pleural cavity lavage
â¸Extracorporeal circulation
43. HYPOTHERMIA
SUMMARY
â¸Minimise further heat loss
â¸Begin rewarming of hypothermic patients early
â¸Some patients are cold and dead but other cold patients who appear dead can
be resuscitated with full neurologic recovery
â¸Endogenous rewarming should occur in moderate-severe hypothermia
â¸Rewarming with forced-air rewarming blankets in most cases of moderate-to-
severe hypothermia can be done without the need to resort to more aggressive
techniques.
â¸Rewarming should be with cardiopulmonary bypass or warm left pleural lavage
in the arrested hypothermic patient.
44. HYPERTHERMIA/HYPOTHERMIA
REFERENCES
â¸Rogers, Ian. Heat-related illness, draft chapter TEXTBOOK OF ADULT EMERGENCY MEDICINE
â¸Heat-Related Illness Emergency Medicine Clinics of North America. Atha, Walter F., MD.. Published
November 1, 2013. Volume 31, Issue 4. Pages 1097-1108.
â¸Drug-Induced Hyperthermic Syndromes. Bryan D. Hayes PharmD, Joseph P. Martinez MD and Fermin
Barrueto MDEmergency Medicine Clinics of North America, 2013-11-01, Volume 31, Issue 4, Pages 1019-
1033,
â¸Hyperthermia Caused by Drug Interactions and Adverse Reactions. Mary S. Paden MD, Lucy Franjic MD and
S. Eliza Halcomb MD. Emergency Medicine Clinics of North America, 2013-11-01, Volume 31, Issue 4, Pages
1035-1044
â¸TEXTBOOK OF ADULT EMERGENCY MEDICINE. 4th Ed. Churchill Livingstone 2015 Elsevier Ltd
â¸Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia. Ken Zafren. Emergency Medicine
Clinics of North America, 2017-05-01, Volume 35, Issue 2, Pages 261-279,
â¸https://www.pharmacytimes.com/contributor/patrick-wieruszewski-bs-pharmd-candidate-
2016/2016/03/pharmacokinetic-and-pharmacodynamic-considerations-for-patients-undergoing-therapeutic-
hypothermia
Editor's Notes
In severe serotonin toxicity and neuroleptic malignant syndrome, increased motor activity and central resetting of the hypothalamic thermostat combine to produce hyperthermia.
Serotonin toxicity: the effects are a consequence of a relative excess of central nervous system serotonin.
Dose related, selective serotonin re-uptake inhibitors (SSRIs), lithium, pethidine, monoamine oxidase inhibitors (MAOIs) and amphetamines.
Neuroleptic malignant syndrome: dopamine depletion or dopamine receptor blockade is responsible
Rare idiosyncratic reaction to neuroleptic agents with an incidence of between 0.02% and 3.0%
Malignant hyperthermia is a genetically inherited disorder in which triggering agents cause a release of sarcoplasmic Ca2+ stores.
Elevated levels of myoplasmic Ca2+ stimulates many intercellular processes, including glycolysis, muscle contraction and an uncoupling of oxidative phosphorylation. Leading to hyperthermia that is purely peripheral in origin.